Possibilities for managing the left ventricular diastolic dysfunction risk in obese patients

Aim. To study the factors preventing the LVDD in obese patients.

Material and methods. The study included 101 obese men who initially did not have LVDD. After 4,7±0,3 years, anthropometric parameters (body mass index (BMI), hip circumference (HC), waist circumference (WC)) and LV diastolic function were reassessed. All patients at the time of enrollment were assessed for the level of neurohumoral (leptin, adiponectin, leptin receptor), pro-inflammatory (tumor necrosis factor-α, interleukin-6, -10, C-reactive protein) and profibrotic factors (collagen type I and III, matrix metalloproteinase-3, vascular endothelial growth factor, transforming growth factor β).

Results. During 4,7±0,3 years of follow-up, 26,7% of the total number inclu­ded in the study registered a decrease in body weight. A tendency to a de­crease in epicardial fat thickness (EFT) by 0,5 mm (7,49 (6,00; 9,00) mm at the time of inclusion and 7,04 (6,00; 9,00) mm over time (p=0,13)). According to echocardiography, LVDD was detected in 20 patients (19,8% after 4,7±0,3 years). Comparative analysis of baseline anthropometric parameters, EFT and after 4,7±0,3 years in groups of patients with (DD+) and without (DD-) LVDD revealed a significant decrease in body weight (p=0,03), BMI (p=0,02), WC (p=0,04) and EFT (p=0,002) only in the DD- group. Patients who developed LVDD initially had increased tumor necrosis factor-α (p=0,02), interleukin-6 (p=0,01), free fatty acids (p=0,001), type I collagen (p=0,001), type III collagen (p=0,02) and a decrease in adiponectin level (p=0,001).

Conclusion. Thus, in patients with a decrease in weight, BMI, WC and EFT during the follow-up period of 4,7±0,3 years, LVDD did not develop, which is associated with a reduced risk of myocardial lipotoxicity against the background of epicardial obesity.

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